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Prolonged muscular flaccidity after stroke. Morphological and functional brain alterations
P Pantano1, R Formisano, M Ricci
1Department of Neurological Sciences, University of Rome La Sapienza, Italy.
Abstract:
Patients with a motor deficit due to ischaemic stroke usually develop muscular spasticity, but in some cases they may remain with a prolonged muscular flaccidity which impairs their recovery. Little is known about the causes of these two different functional outcomes. We correlated CT/MRI and 99mTc HM-PAO SPECT with clinical findings in 42 patients at a mean time interval of 3 months after stroke. The patients were divided into two cohorts with either flaccid (prolonged muscular flaccidity) or spastic (muscular spasticity) hemiparesis. Although patients with prolonged muscular flaccidity had a greater motor deficit, the mean structural volume of the ischaemic lesion was similar to that of the muscular spasticity cohort. There was a significantly higher prevalence of structural involvement of the lentiform nucleus in prolonged muscular flaccidity cases. Relative perfusion in the lentiform nucleus, thalamus and contralateral cerebellar hemisphere was significantly lower in prolonged muscular flaccidity than in muscular spasticity patients. A subgroup with only subcortical structural lesions also showed significantly lower relative perfusion in the ipsilateral frontal association areas. A primary involvement of the lentiform nucleus by the structural lesion seems to be crucial for the persistence of flaccidity after stroke. However, cerebral blood flow (CBF) changes in other structurally intact regions indicate their additional role. It is likely that both subcortical-cortical loops involved in motor control, i.e. cortex-basal ganglia-thalamus-cortex and cortex-pons-cerebellum-thalamus-cortex, are more widely and more severely affected in patients with prolonged muscular flaccidity.
Insights
Prolonged muscular flaccidity after ischemic stroke, unlike spasticity, is linked to lentiform nucleus damage. Reduced blood flow in key motor control areas, including the thalamus and cerebellum, also contributes to flaccidity.
Area of Science:
- Neuroscience
- Neurology
- Radiology
Background:
- Ischemic stroke can lead to motor deficits, typically muscular spasticity, but sometimes prolonged muscular flaccidity, hindering recovery.
- The underlying causes for these divergent functional outcomes post-stroke remain poorly understood.
Purpose of the Study:
- To investigate the neuroanatomical and perfusion correlates of prolonged muscular flaccidity versus muscular spasticity following ischemic stroke.
- To identify specific brain regions and their functional roles in determining post-stroke motor recovery patterns.
Main Methods:
- Correlative analysis of neuroimaging (CT/MRI, 99mTc HM-PAO SPECT) with clinical findings in 42 post-stroke patients.
- Patients categorized into prolonged muscular flaccidity or muscular spasticity hemiparesis cohorts.
- Assessment of lesion volume, structural involvement (especially lentiform nucleus), and relative regional cerebral blood flow (rCBF).
Main Results:
- Mean lesion volume was similar between flaccidity and spasticity groups, despite greater motor deficit in the flaccidity cohort.
- Significantly higher prevalence of lentiform nucleus involvement in the prolonged muscular flaccidity group.
- Lower relative perfusion observed in the lentiform nucleus, thalamus, and contralateral cerebellar hemisphere in flaccidity patients compared to spasticity patients.
- Subgroup analysis revealed reduced ipsilateral frontal association area perfusion in cases with only subcortical lesions.
Conclusions:
- Primary structural damage to the lentiform nucleus appears critical for the persistence of flaccidity after ischemic stroke.
- Altered cerebral blood flow in structurally intact regions, particularly within subcortical-cortical motor loops (basal ganglia and cerebellum pathways), significantly contributes to prolonged flaccidity.
- Both structural integrity and functional perfusion of motor control circuits are crucial for determining post-stroke motor outcomes.